بسم الله الرحمن الرحيم

1. بسم الله الرحمن الرحيم

2. Phylum: Nemathelminthes (Round worms)Class: Nematoda

3. General characters: 1)Separate sexes • Males smaller than females, and commonly has a curved posterior end. 2)Un-segmented, elongated cylindrical, round worms. 3)Body cavity containing body fluid, in which the digestive and genital systems float. 4)Size: varies from less than one mm to nearly one meter in length.

4. 5)The body wall is made up of 3 layers: • Outer laminated non cellular cuticle; which may inflate anteriorly forming cervical alae (Enterobius vermicularis) or posteriorly forming copulatory bursa (Ancytostoma). On the cuticle there may be papillae, expansions or spines. • Thin syncytial layer or hypodermis that secretes the cuticle. • Single muscular layer, divided into 4 quadrants by the hypodermal lines, its arrangement varies in different nematodes and helps in classification.

6. Digestive system:- • A straight tube starting at the anterior head end, by the mouth which is provided with facilities for attachment e.g lips, teeth, and plates which ends by the anus posteriorly. • Mouth leads to oesophagus, with tri-radiate lumen (one dorsal and two subventral) ,varies in shapes according to the species of the nematode parasite, and helps in identification.

8. Types of oesophagus: i-Cellular esophagus: a narrow row of cells attached to the esophagus (Trichocephalus trichiuris , Trichinella spiralis & Capallaria). ii – Muscular: simple tube surrounded with a straited muscular wall: a) One segment: i- Club- shaped oesophagus (Ascaris). ii- Cylindrical esophagus (Filariae)

9. Club- shaped Cylindrical

10. Two segments: 1-Double – bulbed oesophagus, with anterior club shaped portion and posterior spherical part (Oxyuris = Enterobius vermicularis) 2- Rhabditiform oesophagus, with an anterior cylindrical portion and pyriform posterior portion and a narrow constriction in between (Strongyloides stercoralis).

11. Rhabditiform Double – bulbed

12. - After the esophagus is the intestine which proceeds until it opens in the anuson the ventral surface in female or it joins the genital duct which open in cloaca in male (subterminal except in Trichiuris and Trichinella).

13. Reproductive organs: Male: curved posterior end. - In the form of single coiled convoluted tubule, Testes followed by vas deferens, seminal vesicle and finally opens by ejaculatory duct with the anus in the cloaca posteriorly. - The cuticle may show expansion (Copulatory bursa) with or without spicules that help in differentiation.

15. Female: - straight posterior end One or 2 genital systems joining to open by a single vagina in the vulva. - Each has a glandular ovary→ oviduct→ receptaculum seminis →uterus and vagina.

16. Egg of parasitic nematode may hatch in the external environment and controlled by suitable factors as temperature, moisture and oxygen. Or it may hatch after ingested by the host and stimulated by carbon dioxide tension, salts, PH and temperature. In both types larva undergoes 4 molts until it becomes adult.

17. 8 -Excretory system: consists of two longitudinal lateral canals running in the lateral lines . -the lateral canals join in terminal duct→ excretory pore in the region of the oesophagus. 9 - No circulatory system : the fluid in the body cavity contain heamoglobin, glucose, proteins, salts and vitamins that fulfill the function of blood . 10- Nervous system: consists of nerve ring around the esophagus and 6 nerve trunks pass to the head and others to the posterior end. -Sensory organs are in the labial, cervical, anal & genital regions.

18. Transmission of nematodes 1) By ingestion of eggs: • Directly infective when passed in stool (Enterobius). • Infective after a period of maturation outside (Ascaris and Trichocephalus), by the larvated eggs. 2) Ingestion of larvae: • Larva itself: in Trichostrongylus colubriformes and Hookworms through food and drink. • Larva in muscles: Trichina capsule in muscles of pigs. • Larva in insect: Medina worm in cyclops. 3) Penetration of skin: o Larval penetration: Hook worm and Strongyloides. o Insect bite: Filarial worms.

19. Human nematodes are divided according to the habitat of adult worms into: Intestinal nematodes Small intestine: • Ascaris lumbricoides. • Hookworms (Ancylostoma duodenal and Necator americanus). • Strongyloides stercoralis (Dwarf thread worm). • Trichostrongylus colubriformis. • Capillaria philippinensis. • Trichinella spiralis. (considered as both intestinal and tissue nematode).

20. Large intestine: • Enterobius vermicularis. • Trichiuris trichiura. Tissue nematodes • Filariae. • Dracunculus medinensis (Medina worm). • Larva migrans (visceral and cutaneous). • Trichinella spiralis (considered as both intestinal and tissue nematode).

21. Intestinal nematodes1) Ascaris lumbricoides(The giant intestinal round worm) Distribution: • Cosmopolitan (more prevalent) in warm regions with poor sanitation. • Affect all ages but children are more commonly and heavily infected by their frequent exposure to contaminated soil.

22. Adult morphology: • Long cylindrical with tapering ends. • Pink or yellowish creamy in color. • Finely striated cuticle. • Mouth: at the anterior and, with 3 lips; one dorsal and two subventral with a small triangular buccal cavity. Each lip is provided with 2 sensory papillae and fine teeth. • Esophagus: muscular club- shaped followed by the intestine to open in anus in female and cloaca in male.

24. Female: • 20-40 cm × 6 mm • with straight posterior end • two sets of genitalia • vulva at the junction of anterior and middle thirds of the body ventrally. Male: • 15-20 cm × 3 mm • posterior end curved ventrally • one set of genital organs and 2 small equal spicules

26. Ascaris male posterior end

29. Life Cycle: Habitat:the adult worms live free in the small intestine (jejunum). Each female lays 200.000 eggs per day regularly. Its life span is about one year. Definitive host: man. Infective stage: egg containing a second stage rhabditiform larva. Stages in the life cycle: egg in the soil  larvated egg (with 2nd stage rhabditiform larva),  ingested by man larva adult in the small intestine.

31. N.B. The unfertilized eggs are found not only in the absence of males but in about two fifths of all infections, since repeated copulations are necessary for the continuous production of fertile eggs.

32. Ascaris lumbricoides -- the human round worm

33. Ascaris • Fully embryonated eggs are swallowed and L2 hatches in the stomach and penetrate stomach or duodenal mucosa • Larvae enter blood stream and leave through alveoli into lung • Larvae molt several times in the lungs L3/L4 move up and get swallowed • 2-3 months after infection the adult worms start laying eggs (200,000 daily) • Eggs are shed with the feces and embryonate within 2-3 weeks

35. Eggs are voided with stool, mature in the soil after 2 weeks under suitable conditions (25ºc, humidity, shade and oxygen), develops 1st stage Rhabditiform larva within the shell. After one more week, the larva molts into 2nd stage rhabditiform larva within the egg (infective stage).

36. Methods of infection: • Ingestion of mature eggs containing 2nd stage rhabditiform larva, contaminating food (green raw vegetables), water or hands. Cockroaches and house flies may carry the larvated eggs to human food (mechanical transmission). • Inhalation of mature eggs to the nasopharynx.

37. - Egg hatches in the small intestine, liberating the larva (freshly laid eggs with no larva inside are not capable of causing infection). - Rhabditiform larva comes out of the egg to the lumen of the small intestine, penetrate the mucosa to reach the circulation, carried to the right side of the heart  pulmonary arteries  lung. The larva breaks out of capillaries into lung alveoli and moults twice (2nd and 3rd moults).

38. - The larva creeps along the bronchioles  bronchi  trachea  larynx  pharynx, then swallowed to reach the small intestine where it moults once (4th moult and becomes adult). - Eggs appear in feaces 2-3 months after infection. - The life span of a female Ascaris in human body is about one year, then dies. So if a person shows infection with Ascaris for several years, it only means that this person is continuously re-infected.

39. N.B. In massive infection, some larvae may reach the general circulation to be filtered in various organs as abnormal foci in: lymph glands, spleen, kidneys, brain or spinal cord. When reaching the kidney they may find their way to urine and attract attention. In such ectopic sites, larvae are unable to grow to maturity and most of them are destroyed.

40. Pathogenesis and Clinical Manifestations Disease: Ascariais: The usual infection consisting of 5 – 10 worms, often goes unnoticed by the host and is discovered on a routine stool examination or by the discovery of an adult worm passed spontaneously in stool. The pathogenic effects of ascariasis are due to the following mechanisms: Allergic reactions to the parasitic stages. Effect of the adult on host nutrition. Mechanical effect of the adult worm. Wandering larvae and adults. Microorganisms carried with larvae during migration.

41. Migrating larvae: • Lung:In light infection, there is slight damage with unnoticed pathological lesions. In heavy infection, the migrating larvae in the lungs result in lobular pneumonitis, there is cellular infiltration, serous exudates and some haemorrhage causing cough and bronchial irritation, (asthmatic attack), expectoration with blood stained sputum and aedema of lips, microscopically the larvae may be detected in the sputum, with many oesinophils. 2.General circulation: Occasionally some larvae reach the general circulation and distributed to various organs as lymph nodes, brain, spleen & kidneys (ectopic sites) leading to abnormal clinical manifestations as a result of visceral larva migrans

42. Adult worm: in the intestine may cause abdominal discomfort with distension, colic, diarrhea or constipation, vomiting and dyspepsia due to production of anti-enzymes (anti-peptic and anti- tryptic substances that interfere with protein digestion). • Traumatic effects: • In heavy infection  intestinal obstruction. • Obstruction of the bile ducts by the worms  obstructive jaundice. • Appendix  appendicitis. • Obstruction of ampulla of Vater  acute hemorrhagic pancreatitis. • Perforation of intestinal wall  peritonitis.

43. Some worms may ascend via the stomach and oesophagus to the nasopharynx, enter the larynx causing suffocation especially in children. It may come out of mouth or nose or even go to Eustachian tube from the pharynx resulting in damage of the middle ear. Toxic effects: metabolic by -products of living or dead worms may give rise to fever, allergic manifestations (urticaria and asthma) and nervous irritability (insomnia and even convulsions) Nutritional impact: loss of appetite  malnutrition and impairment of growth, with vitamin A and C deficiency.

44. Ascaris • Infection depends on fecal contamination of food, water or soil • Eggs are sensitive to sun light but otherwise extraordinarily resistant (ascarosides - special glycolipids secreted by the embryo) • Fertilized eggs are shorter and rounder than unfertilized

45. Ascaris • Occasional pulmonary symptoms • Intestinal phase mostly asymptomatic, but worms can lead to malnourishment in children • Dangerous complications are mostly observed in children under 10 • Volvulus, a mass of knotted worms obstructing the intestine • Penetration of the bile duct and liver by adult worms • Penetration of the intestinal wall, followed by peritonitis • Wandering and obstruction can be linked to certain medications

46. Diagnosis • Clinical: symptom of intestinal ascariasis are indistinguishable from those of other intestinal helminthic infections. • Laboratory • Detection of eggs in stool. (direct smear, after concentration, Stoll’s technique). • Detection of migrating larvae in sputum or better in gastric lavage contents. • Detection of adults passing out with or without stool or in vomitus. • Eosinophilia (7 – 12%). • Radiology: Barium meal shows cylindrical filling defect (string sign). • Biopsy.

47. Treatment Drugs Levamizol hydrochloride (Ketrax): 2 mg/kg as a single oral dose Mebendazole (Antiver, vermox) or Flubendazole (Fluvermal). Piperazine citrate, hydrate or adipate (parazine, vermizine or uvilon). Surgical For treatment of complications e.g intestinal obstruction, obstruction of appendix or bile ducts.

48. Control Mass treatment of infected persons. Sanitary disposal of excreta. Health education. Cleanliness (washing hands before meal). Proper washing of green raw vegetables. Pure water supply. Control of flies and other insects. Stool should not be used as a fertilizer unless being treated by chemicals or temperature of 50°C or higher to kill eggs.

50. Toxocara canis & Toxocara catiThese two species are ascarid parasites of dogs and cats. They are cosmopolitan. Both are similar in biology and morphology • Adult Toxocara has three lips and a pair of cervical alae. Mature male: 4-6 cm. Mature female: 6-10 cm. • Toxocara eggs: Dark brown with pitted shells Size: 85 × 75  Passes immature in dogs’ stool.